Recent research also suggests that hyperphosphorylated Tau induces free radical production and lipid peroxidation and reduces antioxidant enzymes (e.g., glutathione peroxidase and catalase), causing an imbalance between the production of free radicals and endogenous antioxidant enzymes, ultimately leading to mitochondrial dysfunction in AD and other tauopathies [34,38,39,40]. The gene discussed is MAPT; the disease is Alzheimer disease.